| First Author | Carè A | Year | 2007 |
| Journal | Nat Med | Volume | 13 |
| Issue | 5 | Pages | 613-8 |
| PubMed ID | 17468766 | Mgi Jnum | J:121893 |
| Mgi Id | MGI:3712603 | Doi | 10.1038/nm1582 |
| Citation | Care A, et al. (2007) MicroRNA-133 controls cardiac hypertrophy. Nat Med 13(5):613-8 |
| abstractText | Growing evidence indicates that microRNAs (miRNAs or miRs) are involved in basic cell functions and oncogenesis. Here we report that miR-133 has a critical role in determining cardiomyocyte hypertrophy. We observed decreased expression of both miR-133 and miR-1, which belong to the same transcriptional unit, in mouse and human models of cardiac hypertrophy. In vitro overexpression of miR-133 or miR-1 inhibited cardiac hypertrophy. In contrast, suppression of miR-133 by 'decoy' sequences induced hypertrophy, which was more pronounced than that after stimulation with conventional inducers of hypertrophy. In vivo inhibition of miR-133 by a single infusion of an antagomir caused marked and sustained cardiac hypertrophy. We identified specific targets of miR-133: RhoA, a GDP-GTP exchange protein regulating cardiac hypertrophy; Cdc42, a signal transduction kinase implicated in hypertrophy; and Nelf-A/WHSC2, a nuclear factor involved in cardiogenesis. Our data show that miR-133, and possibly miR-1, are key regulators of cardiac hypertrophy, suggesting their therapeutic application in heart disease. |
